PharmaBiotec Research Center, Institute of Neurobiology, University of Aarhus, Denmark PharmaBiotec Research Center, Department of Anatomy, Institute of Medical Biology, University of Odense, Denmark.
Restor Neurol Neurosci. 1994 Jan 1;6(3):239-49. doi: 10.3233/RNN-1994-6307.
Fascia dentata tissue blocks from newborn rats were grafted into one-week-old, ibotenic acid-induced lesions of the fascia dentata, or the normal fascia dentata of adult rats. After at least 2 months survival the recipient rats were subjected to 10 min of forebrain ischemia (4-vessel occlusion), and examined 2 or 4 days later for neuronal degeneration in the host hippocampi and the transplants, by silver staining and immunohistochemistry. Transplants survived well in both normal and lesioned host brains, with easily recognizable subfields and layers and presence of normal types of principal and non-principal neurons. As expected, argyrophilic, degenerating neurons were present in the pyramidal cell layer of CAl and CA3c of the non-grafted contralateral host hippocampus and in the contralateral dentate hilus (CA4). In the hilus the degeneration corresponded to the loss of somatostatin-immunoreactive neurons, while parvalbumin-immunoreactive neurons were spared. In the dentate transplants degenerating neurons were observed in the granule cell layer, the hilus and the adjacent CA3 pyramidal cell layer. There was no obvious loss of either somatostatin- or parvalbumin-immunoreactive neurons. The degeneration varied considerably between transplants, from a few to large groups of silver stained neurons, but this difference did not display any obvious relation to grafting into normal or lesioned hosts, the exact location of the grafts or the general organization and distribution of intrinsic or extrinsic host afferents in the grafts. The results demonstrate that both ischemia-susceptible and -resistant types of neurons grafted to normal and lesioned adult rat brains are susceptible to transient forebrain ischemia after transplantation. In spite of an extensive reorganization of transplant nerve connections, the physiologicalbiochemical mechanisms necessary for the induction of ischemic cell death were accordingly present in the transplants.
将新生大鼠的齿状回组织块移植到新生大鼠的齿状回内的海人酸诱导损伤部位或成年大鼠的正常齿状回中。在至少 2 个月的存活期后，接受者大鼠接受 10 分钟的全脑缺血（四血管闭塞），并在 2 或 4 天后通过银染色和免疫组织化学检查宿主海马和移植物中的神经元变性。移植物在正常和损伤的宿主脑中均存活良好，具有易于识别的亚区和层，并且存在正常类型的主神经元和非主神经元。如预期的那样，在未移植的对侧宿主海马体的 CA1 和 CA3c 的锥体细胞层以及对侧齿状回门（CA4）中存在银染的、退化的神经元。在门部，变性与生长抑素免疫反应性神经元的丧失相对应，而副甲状腺素免疫反应性神经元则幸免。在齿状回移植物中，在颗粒细胞层、门部和相邻的 CA3 锥体细胞层中观察到退化的神经元。生长抑素或副甲状腺素免疫反应性神经元均无明显丢失。退化在移植物之间变化很大，从少数到大量的银染神经元，但这种差异与移植到正常或损伤的宿主、移植物的确切位置或移植物中固有或外在宿主传入的一般组织和分布没有明显的关系。结果表明，移植到正常和损伤的成年大鼠脑中的缺血敏感和耐受型神经元在移植后均易发生短暂性全脑缺血。尽管移植神经连接发生了广泛的重组，但诱导缺血性细胞死亡所需的生理生化机制在移植物中仍然存在。
